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Y. Iijima, T. Ito, T. Oikawa, M. Eguchi, M. Eguchi-Ishimae, N. Kamada, K. Kishi, S. Asano, Y. Sakaki, and Y. Sato, “A New ETV6/TEL Partner Gene ARG(ABL-Related Gene or ABL2), Identified in an AML-M3 Cell Line with a t(1;12)(q25;p13) Translocation,” Blood, Vol. 95, 2000, pp. 2126-2131.

has been cited by the following article:

• TITLE: Distinct Transforming Activity of ABL Family Tyrosine Kinase Oncogenes Is Induced by Their C-Terminal Domain*

  AUTHORS: Keiko Okuda, Hideyo Hirai

  KEYWORDS: Leukemia; Chimeric Oncogene; ABL Family Tyrosine Kinase; Signal Transduction

  JOURNAL NAME: Open Journal of Blood Diseases, Vol.3 No.3A, November 4, 2013

  ABSTRACT: The TEL/ARG oncogene is similar in structure to the TEL/ABL fusion found in human leukemia, however, we have demonstrated previously that the expression of TEL/ARG in Ba/F3 cells does not sustain strong activity of proliferation, whereas, that of TEL/ABL appeared to induce immediate cell proliferation. To study the molecular basis of the difference in the transforming activity of TEL/ARG and TEL/ABL, TEL/ARG mutants that swapped the kinase domain or C-terminus of ARG with the corresponding domain in ABL were generated, and each mutant was expressed in Ba/F3 cells. A TEL/ARG mutant containing the ABL kinase domain was similar to TEL/ARG in this study, but replacing the ARG C-terminal domain with that of ABL resulted in accelerated proliferation that was similar to that of TEL/ABL. When expressed in primary mouse bone marrow cells by retroviral transduction, spontaneous colony formation in methylcellulose culture was observed, in a fashion dependent on the C-terminal portion of ABL. These results indicate that distinct bio-phenotypes associated with these oncogenes are likely to be regulated by their C-termini, and the C-terminus of ARG contains a functional subdomain that impairs the growth signal induced by ABL family tyrosine kinase.